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Validated All-in-One™ qPCR Primer for KLF2(NM_016270.3) Search again
Product ID:
HQP090427
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
LKLF
Gene Description:
KLF transcription factor 2
Target Gene Accession:
NM_016270.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Gene References into function
- LKLF is the first endothelial transcription factor that is uniquely induced by flow and might therefore be at the molecular basis of the physiological healthy, flow-exposed state of the endothelial cell
- KLF2 has a role as a negative regulator of adipogenesis
- KLF2 is a novel regulator of endothelial activation in response to proinflammatory stimuli.
- LKLF may establish a phenotype that primes quiescent cells for responses to specific extracellular stimuli.
- The ability to differentially modulate key molecules such as TM, eNOS, PAI-1, & TF identifies KLF2 as an important regulator of endothelial coagulant function. KLF2 is a "molecular switch" regulating important aspects of vascular function.
- Level of WEE1 is regulated by KLF2 and enhanced KLF2 expression sensitizes cells to DNA damage-induced apoptosis.
- a promoter element activated by a PI3kinase-dependent chromatin-remodeling pathway induces KLF2
- demonstrated that KLF2 transcription factor is necessary for the statin-mediated regulation of several pathophysiologically relevant genes
- KLF2 has roles in primitive erythropoiesis and regulating human and murine embryonic beta-like globin genes
- KLF2 is a regulator of VEGFR2/KDR and has a role in regulating angiogenesis
- In co-transfection assays in K562 cells, it was demonstrated that KLF2, 5 and 13 positively regulate, and KLF8 negatively regulates, the gamma-globin gene through the CACCC promoter element.
- Statin-dependent induction of eNOS and thrombomodulin requires KLF2 and thereby provides a novel molecular target for modulating endothelial function in vascular disease.
- KLF2 regulates IL-2 promoter activity in the earliest stages of T cell activation.
- KLF2 is selectively induced in endotheliums by atheroprotective flow via a MEK5/ERK5/MEF2 signaling pathway. Expression of KLF2 results in the regulation of endothelial programs controlling inflammation, thrombosis, vascular tone, and angiogenesis.
- KLF2 acts as a central transcriptional switch point between the quiescent and activated states of the adult endothelial cell
- findings demonstrate that different flow patterns differentially regulate the expression of KLF2 and that KLF2 has an anti-apoptotic effect
- nucleolin binds the KLF2 promoter
- KLF2 expression in circulating monocytes is reduced in patients with chronic inflammatory conditions such as coronary artery disease.
- Human transcription factors KLF2 and KLF6 are targets of the P. aeruginosa type III exoenzymes S and Y, with potential importance in host cell death.
- Shear stress and KLF2 inhibit nuclear activity of ATF2, providing a potential mechanism by which endothelial cells exposed to laminar flow are protected from basal proinflammatory, atherogenic gene expression.
- analysis of SNPs, located in the KLF2, KLF4 and KLF5 gene did not show an association with Type 2 diabetes in this French population
- Atorvastatin-mediated HO-1 upregulation, and its associated antioxidant effect, are KLF2-dependent.
- Simvastatin has a strong anti-inflammatory effect on monocytes including upregulation of the atheroprotective factor KLF-2.
- Data suggest that, in neutrophil-dominated airway environments, such as that seen in cystic fibrosis, reduced LKLF activity releases a brake on pro-inflammatory cytokine production and may contribute to the inflammatory responses seen in CF.
- up-regulation of CD59 via ERK5/KLF2 activation leads to endothelial resistance to complement-mediated injury and protects from atherogenesis in regions of laminar shear stress
- KLF2 substantially enhances antioxidant activity of Nrf2 by increasing its nuclear localization and activation.
- downregulation of antiinflammatory factors, such as TNFAIP3, KLF2, ZFP36, and BTG1, seems to be involved in acceleration of immune response, thus exacerbation of acute GVHD.